The aim of this proposal is to test the controversial hypothesis that in the adult dog, myocardial cellular hyperplasia may be a contributing factor in the enlarged hearts produced by atrioventricular block and electronic pacing. In this model, myocardial cell size - the true index of myocardial hypertrophy - did not increase. In order to eliminate the possiblity of focal occurrences of myocardial cellular hypertrophy to account for the increase in heart weight, we propose to quantitate cell size in the subepicardial, central, and subendocardial layers of the basal, midwall, and apical regions from the left and right ventricular free walls and septum and papillary muscles at various times after stress. In addition, we propose to quantitatively measure edema, fibrosis and myocyte concentration. In order to eliminate electronic pacing as a causative factor in the production of myocyte hyperpasia, the above studies will be performed in a group of dogs with complete block and compared with a subgroup which will be paced at a rate 3 to 5 bpm above the blocked ventricular rate. In order to eliminate electronic pacing as a causative factor in the production of myocyte hyperplasia, the above studies will be performed in a group of dogs with complete block and compared with a subgroup which will be paced at a rate 3 to 5 bpm above the blocked ventricular rate. To determine whether myocyte hyperplasia can be produced by other stresses resulting in increased ventricular weight, the above aims will be performed in the pressure and volume overloaded models.